The basis for the exaggerated release of substrates for gluconeogenesis and other caloric fuels in Reye's syndrome, a pediatric disorder characterized by encephalopathy and fatty visceral changes, will continue to be explored using the fat cell as a model system since excessive lipolysis is a prominent feature of this disorder. The process of lipolysis is being studied in biopsied tissues and the sequential steps involved in the transmission of a lipolytic stimulus is being examined and compared in control and Reye's samples. The molecular forms of liver PDE from affected and age-matched controls are also being isolated and characterized. Pancreatic endocrine responses to various modulators in survivors and family members are under investigation to determine the basis for an altered responsiveness to metabolic stress observed in these subjects.